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Abstract

Elevated endocannabinoid levels are linked with the development of atherosclerotic vascular disease and coronary circulatory dysfunction in obese individuals, a precursor of coronary artery disease. However, it remains unclear whether endocannabinoid levels represent a risk factor or diagnostic biomarker for acute atherosclerotic vascular events. So far, a causal role of increased endocannabinoid levels in atherosclerotic plaque vulnerability and occurrence of acute clinical events has not been investigated. Here, we studied the involvement of fatty acid amide hydrolase (FAAH) deficiency, the major enzyme responsible for endocannabinoid anandamide degradation, in atherosclerotic plaque vulnerability.